miR‐29a attenuates cardiac hypertrophy through inhibition of PPARδ expression

Although cardiac hypertrophy is widely recognized as a risk factor that leads to cardiac dysfunction and, ultimately, heart failure, the complex mechanisms underlying cardiac hypertrophy remain incompletely characterized. The nuclear receptor peroxisome proliferator‐activated receptor δ (PPARδ) is i...

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Veröffentlicht in:Journal of cellular physiology 2019-08, Vol.234 (8), p.13252-13262
Hauptverfasser: Zhang, Si, Yin, Zhongnan, Dai, Fei‐Fei, Wang, Hao, Zhou, Meng‐Jiao, Yang, Ming‐Hui, Zhang, Shu‐Feng, Fu, Zhi‐Feng, Mei, Ying‐Wu, Zang, Ming‐Xi, Xue, Lixiang
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Sprache:eng
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Zusammenfassung:Although cardiac hypertrophy is widely recognized as a risk factor that leads to cardiac dysfunction and, ultimately, heart failure, the complex mechanisms underlying cardiac hypertrophy remain incompletely characterized. The nuclear receptor peroxisome proliferator‐activated receptor δ (PPARδ) is involved in the regulation of cardiac lipid metabolism. Here, we describe a novel PPARδ‐dependent molecular cascade involving microRNA‐29a (miR‐29a) and atrial natriuretic factor (ANF), which is reactivated in cardiac hypertrophy. In addition, we identify a novel role of miR‐29a, in which it has a cardioprotective function in isoproterenol hydrochloride‐induced cardiac hypertrophy by targeting PPARδ and downregulating ANF. Finally, we provide evidence that miR‐29a reduces the isoproterenol hydrochloride‐induced cardiac hypertrophy response, thereby underlining the potential clinical relevance of miR‐29a in which it may serve as a potent therapeutic target for heart hypertrophy treatment. MicroRNA‐29a (miR‐29a) may play a crucially protective role in the process of cardiac hypertrophy, and this role is likely achieved via the suppression of nuclear receptor peroxisome proliferator‐activated receptor δ and subsequent decreased expression of atrial natriuretic factor.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.27997